Chronic myeloid leukemia: from molecular mechanisms to targeted treatment and clinical outcomes

Chronic Myeloid Leukemia (CML) is a type of blood cancer characterized by the uncontrolled production of myeloid cells, primarily driven by the BCR-ABL fusion gene formed from the Philadelphia chromosome translocation. This paper provides a comprehensive overview of CML, beginning with its underlying molecular mechanisms and progressing through its epidemiology, diagnosis, staging, prognosis, and treatment. The BCR-ABL protein plays a central role in disease development by continuously signaling cells to divide and avoid apoptosis, ultimately disrupting normal hematopoiesis. Advances in diagnostic methods, particularly molecular techniques such as polymerase chain reaction, have improved the ability to detect and monitor disease progression over time. The introduction of tyrosine kinase inhibitors (TKIs) has significantly changed the clinical course of CML, allowing many patients to manage the disease as a chronic condition with improved survival and quality of life. Prognosis is closely linked to the phase of the disease at diagnosis and the depth of molecular response achieved during treatment. Ongoing research, including the development of next-generation targeted therapies and immunotherapy approaches, continues to expand treatment options and address challenges such as drug resistance. Overall, CML serves as a strong example of how advances in molecular medicine can lead to more precise and effective cancer treatments.